Effects of vasoconstriction on the acute anterior pituitary hormonal response to head injury

WOS: 000178883400008PubMed: 12372703Since cerebral vasoconstriction alone may impair the hypothalamic and pituitary circulation, we planned to investigate whether the hormonal response to the vasoconstriction that may be induced by the head injury is a significant component of the general acute hormonal response to head injury. Although diffuse adrenocorticotropic hormone immunohistochemical staining of the adenohypophysis of rabbits was observed in the head trauma administered group, only mild positive staining was present in the Endothelin-1 administered group. However, decreased prolactin staining was found in both of the groups. It is postulated that trauma induced vasoconstriction may not be an important manipulating factor in the corticotrophic hormone response to injury, while it may be responsible for the decreased prolactin response. (C) 2002 Elsevier Science Ltd. All rights reserved

Effects of trauma and pain on the acute anterior pituitary hormonal response

PubMed: 12147213The aim of this study was to compare the effects of trauma and pain on the pituitary gland so as to determine whether pain is a significant component in the general acute hormonal trauma response. Adenohypophysis of rabbits that have undergone either diffuse traumatic brain injury or pain were investigated using immunohistochemistry. The ACTH staining pattern of the pain-administered rabbits was not as strong as the head-trauma-administered group, whereas PRL staining pattern of the former group was not so weak as the later group. As a conclusion, since adrenocorticotrophic hormone and prolactin staining patterns were different in the trauma administered and pain induced groups; it may be postulated that pain alone may not be an important factor in the hormonal response to trauma. © 2002 Published by Elsevier Science Ltd

Investigation of the effect of hyperbaric oxygen on experimental cyclosporine nephrotoxicity

Hyperbaric oxygen interacts with drugs which patients use concurrently with hyperbaric oxygen treatment, which may cause in potentiation or inhibition of both therapeutic and toxic effects. We examined the effect of hyperbaric oxygen therapy on experimental cyclosporine A nephrotoxicity. The study comprised four groups of rats: a control group, a cyclosporine A group (25 mg/kg/day intraperitoneally for four days), a hyperbaric oxygen group (60 min. every day for four days at 2.5 atmospheric pressure), and a cyclosporine A+hyperbaric oxygen group (CsA 25 mg/kg/day intraperitoneally for four days+hyperbaric oxygen for 60 min. every day for four days at 2.5 atmospheric pressure). Hyperbaric oxygen did not alter biochemical parameters. Cyclosporine A increased serum urea and serum creatinine levels and decreased creatinine clearance. In the cyclosporine A+hyperbaric oxygen group serum urea level increased more than in the cyclosporine A group. Cyclosporine A increased tubular epithelial cell apoptosis and necrosis score values. The numbers of apoptotic cells in proximal tubule epithelial cells in the cyclosporine A+hyperbaric oxygen group were significantly higher than those of the cyclosporine A group. We recommend that renal functions of the patients receiving cyclosporine A should be monitored during hyperbaric oxygen therapy

A retrospective analysis for aetiology and clinical findings of 287 secondary amyloidosis cases in Turkey

Background. Secondary amyloidosis is the most frequent of the various types of systemic amyloidosis, the epidemiology of which is not yet fully known. The aim of our study was to evaluate retrospectively the collective data for the aetiological distribution, clinical findings and approaches to the management of secondary amyloidosis in Turkey